We audited the relationship between obesity and the age at which hip and knee replacement was undertaken at our centre. The database was analysed for age, the Oxford hip or knee score and the body mass index (BMI) at the time of surgery. In total, 1369 patients were studied, 1025 treated by hip replacement and 344 by knee replacement. The patients were divided into five groups based on their BMI (normal, overweight, moderately obese, severely obese and morbidly obese). The difference in the mean Oxford score at surgery was not statistically significant between the groups (p > 0.05). For those undergoing hip replacement, the mean age of the morbidly obese patients was ten years less than that of those with a normal BMI. For those treated by knee replacement, the difference was 13 years. The age at surgery fell significantly for those with a BMI > 35 kg/m(2) for both hip and knee replacement (p > 0.05). This association was stronger for patients treated by knee than by hip replacement.

No abstract

Current understanding of adaptive immune, particularly T cell, responses to human rhinoviruses (RV) is limited. Memory T cells are thought to be of a primarily T helper 1 type, but both T helper 1 and T helper 2 memory cells have been described, and heightened T helper 2/ lessened T helper 1 responses have been associated with increased RV-induced asthma exacerbation severity. We examined the contribution of T helper 1 cells to RV-induced airways inflammation using mice deficient in the transcription factor T-Box Expressed In T Cells (Tbet), a critical controller of T helper 1 cell differentiation. Using flow cytometry we showed that Tbet deficient mice lacked the T helper 1 response of wild type mice and instead developed mixed T helper 2/T helper 17 responses to RV infection, evidenced by increased numbers of GATA binding protein 3 (GATA-3) and RAR-related orphan receptor gamma t (RORγt), and interleukin-13 and interleukin-17A expressing CD4+ T cells in the lung. Forkhead box P3 (FOXP3) and interleukin-10 expressing T cell numbers were unaffected. Tbet deficient mice also displayed deficiencies in lung Natural Killer, Natural Killer T cell and γδT cell responses, and serum neutralising antibody responses. Tbet deficient mice exhibited pronounced airways eosinophilia and mucus production in response to RV infection that, by utilising a CD4+ cell depleting antibody, were found to be T helper cell dependent. RV induction of T helper 2 and T helper 17 responses may therefore have an important role in directly driving features of allergic airways disease such as eosinophilia and mucus hypersecretion during asthma exacerbations.

No abstract